BACTERIAL DIARRHEAS

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BACTERIAL DIARRHEAS:

BACTERIAL DIARRHEAS BY DR SHASHIDHAR

Definition :

Definition Stool weight in excess of 200 gm/day 3 or more loose or watery stools/day Alteration in normal bowel movement characterized by decreased consistency and increased frequency Less than 14 days in duration

Infectious Diarrhea:

Infectious Diarrhea 3-5 billion episodes yearly Major cause of worldwide morbidity and mortality 5 million deaths yearly, 80% < 1 year of age Major cause of work/school absenteeism Major economic burden, especially in developing countries

Etiology:

Etiology Viral : 70-80% of infectious diarrhea in developed countries Bacterial : 10-20% of infectious diarrhea but responsible for most cases of severe diarrhea Protozoan : less than 10%

CAUSES OF ACUTE DIARRHOEA:

CAUSES OF ACUTE DIARRHOEA INFECTIOUS NONINFECTIOUS

INFECTIOUS:

INFECTIOUS TOXIN MEDIATED Bacillus cereus Staphylococcal enterotoxin Clostridial spp. enterotoxin Scombrotoxic

Infective food poisoning:

Infective food poisoning Rotavirus gastroenteritis Campylobacter Salmonella Verocytotoxigenic E. coli Other E. coli, e.g. travellers' diarrhoea Shigella Clostridium difficile Norovirus Cholera

PROTOZOAL:

PROTOZOAL Giardiasis Amoebic dysentery Cryptosporidium Isosporiasis Microsporidiosis

SYSTEMIC ILLNESS:

SYSTEMIC ILLNESS Sepsis Meningococcal sepsis Pneumonia Malaria

NON INFECTIOUS:

NON INFECTIOUS Gastrointestinal Acute diverticulitis Inflammatory bowel disease  Ulcerative colitis Crohn's disease Bowel malignancy Pelvic inflammatory disease Overflow from constipation

METABOLIC UPSET:

METABOLIC UPSET Ketosis (e.g. diabetic decompensation ) Vasoactive intestinal peptide release Carcinoid syndrome Uraemia

DRUGS & TOXINS:

DRUGS & TOXINS NSAIDs Cytotoxic agents Antibiotics Ciguatera fish poisoning Dinoflagellates Plant toxins Heavy metals

CAUSES OF BLOODY DIARRHOEA:

CAUSES OF BLOODY DIARRHOEA INFECTIOUS NON INFECTIOUS

INFECTIOUS CAUSES:

INFECTIOUS CAUSES Campylobacter spp Shigella dysentery Non- typhoidal salmonellae Enterohaemorrhagic E. coli Entero -invasive E. coli Clostridium difficile Vibro parahaemolyticus Entamoeba histolytica (amoebic dysentery)

NON INFECTIOUS CAUSES:

NON INFECTIOUS CAUSES Diverticular disease Rectal or colonic malignancy Inflammatory bowel disease Bleeding haemorrhoids Anal fissure Ischaemic colitis Intussusception

These organisms cause diarrhea through a wide variety of mechanisms:

These organisms cause diarrhea through a wide variety of mechanisms Pathophysiology Osmotic Secretory Exudation Abnormal motility

Osmotic Diarrhea:

Osmotic Diarrhea Interferes with absorption of water Solutes are ingested (fasting stops diarrhea) Magnesium sulfate or citrate or magnesium containing antacids Sorbitol Malabsorption of food Lactase deficiency Celiac sprue Variety of infectious organisms (particularly viruses) Definition: Increased amounts of poorly absorbed, osmotically active solutes in gut lumen

Secretory Diarrhea:

Secretory Diarrhea Excess secretion of electrolytes and water across mucosal surface Usually coupled with inhibition of absorption Clinical features stools very watery stool volume large fasting does not stop diarrhea

Secretory Diarrhea:

Secretory Diarrhea Bacterial or viral enterotoxins Cholera, enterotoxigenic E. coli , B. cereus , S. aureus, Rotavirus, Norwalk virus Hormonal secretagogues Certain laxatives (castor oil, senna) Other causes

Exudative Diarrhea:

Exudative Diarrhea Intestinal or colonic mucosa inflamed and ulcerated Leakage of fluid, blood, pus Impairment of absorption Increased secretion (prostaglandins) The extent and location of bowel involved determines Severity of diarrhea Systemic signs and symptoms (abdominal pain, fever, leukocytosis, etc) Tenesmus, urgency

Exudative Diarrhea:

Exudative Diarrhea Infectious, invasive organisms Shigella, Campylobacter, Yersinia, E. histolytica, EIEC, C diff CMV Idiopathic inflammatory bowel disease Crohns disease Ulcerative Colitis Ischemia

Invasive organisms produce leukocytes and blood in stool:

Invasive organisms produce leukocytes and blood in stool A laboratory equivalent of this is the presence of lactoferrin in a sample of stool

Abnormal Motility:

Abnormal Motility Increased colonic motility Irritable bowel syndrome Increased small bowel motility Hyperthyroidism, post-operative dumping Decreased small bowel motility Scleroderma, with bacterial overgrowth Anal sphincter dysfunction Incontinence

Diarrhea:

Diarrhea Non-inflammatory Watery diarrhea, no blood or mucus or pus in stool, no fever or systemic signs Secretory or osmotic mechanism Dehydration may occur Generally self-limited and more benign Therapy generally supportive Inflammatory Frequent lower volume stool, mucoid, bloody, or purulent. Often with fever or systemic signs, tenesmus, urgency Exudative mechanism Dehydration rare Less benign

History:

History Onset and duration of diarrhea Timing of exposure to potential pathogens Travel, ingestion history, environment, recent medications (antibiotics), age Character of stool Volume, presence of blood, mucus, or pus Associated symptoms and signs Abdominal pain, fever, vomiting, dehydration

Physical examination:

Physical examination Vital signs: Fever, tachycardia Abdominal tenderness or pain Signs of dehydration Blood, mucus, or pus in stool

ASSESSMENT OF DEHYDRATION:

ASSESSMENT OF DEHYDRATION

ASSESSMENT OF DEHYDRATION (contd.):

ASSESSMENT OF DEHYDRATION (contd.)

ASSESSMENT OF DEHYDRATION (contd.):

ASSESSMENT OF DEHYDRATION (contd.)

Evaluation of diarrhea:

Evaluation of diarrhea How long has the diarrhea been present? Was it acquired in a particular environment? Hospital Recent antibiotic use While traveling Day care, cruise ship, picnic, etc Exposure to sick persons What are the characteristics of the diarrhea Is there blood, mucus, or pus in the stool Is it high volume or low volume Is there associated tenesmus or urgency What are the associated symptoms? Fever, abdominal pain, vomiting, dehydration

Is evaluation required in every patient?:

Is evaluation required in every patient? No Evaluate those with high fever, systemic illness, tenesmus, blood/pus in stool, dehydration, immunocompromised Remainder can often be managed without specific diagnosis with rehydration and antiperistaltic agents

Evaluation of Infectious Diarrhea:

Evaluation of Infectious Diarrhea Stool studies fecal leukocytes and RBC/blood Bacterial culture Include C. difficle toxin assay May need to request EHEC screen Endoscopic evaluation may be useful in some especially for bloody diarrhea or chronic diarrhea

Stool Characteristics and Determining Their Source :

Stool Characteristics and Determining Their Source Stool Characteristics Small Bowel Large Bowel Appearance Watery Mucoid and/or bloody Volume Large Small Frequency Increased Highly increased Blood Possibly positive but never gross blood Commonly grossly bloody pH Possibly <5.5 >5.5 Reducing substances Possibly positive Negative WBCs <5/high power field Commonly >10/high power field Serum WBCs Normal Possible leukocytosis , bandemia

PowerPoint Presentation:

Organisms Viral Rotavirus Adenovirus Calicivirus Astrovirus Norovirus Invasive bacteria Escherichia Coli ( enteroinvasive , enterohemorrhagic ) Shigella species Salmonella species Campylobacter species Yersinia species Aeromonas species Plesiomonas species Enterotoxigenic bacteria E coli Klebsiella Clostridium perfringens Cholera species Vibrio species Toxic bacteria Clostridium difficile Parasites Giardia species Cryptosporidium species Parasites Entamoeba organisms Stool Characteristics Small Bowel Large Bowel

Fecal PMNs:

Fecal PMNs Common in Shigella, Campylobacter , EIEC, C. diff Less common in Salmonella, Yersinia, ETEC, EAEC Now largely replaced with fecal lactoferrin

Treatment of Diarrhea:

Treatment of Diarrhea Treatment of specific etiology Non-specific treatment hydration Absorptions (Kaopectate®) Bismuth Antiperistaltics/opiate derivatives Fiber supplementation

COMPOSITION OF ORS:

COMPOSITION OF ORS

AMOUNT OF SALT LOSS DURING DIARRHEA :

AMOUNT OF SALT LOSS DURING DIARRHEA

Oral rehydration solutions:

Oral rehydration solutions

PowerPoint Presentation:

When and What : Considerations for antibiotics for acute diarrhea

Why not treat everyone with bacterial diarrhea?:

Why not treat everyone with bacterial diarrhea? Some have no effective specific treatment Treatment may not change disease duration or severity Treatment may predispose to carrier state Treatment may produce complications (HUS, antibiotic resistance, C. difficle , toxic megacolon )

Who should be treated?:

Who should be treated? Antibiotics indicated Antibiotics indicated if Severely ill immunocompromised Antibiotics not indicated Shigella Campylobacter EHEC ETEC Yersinia viruses V. cholera EAEC C. diff Salmonella

PATHOPHYSIOLOGY:

PATHOPHYSIOLOGY Diarrhea is the reversal of the normal net absorptive status of water and electrolyte absorption to secretion. OSMOTIC DIARRHEA SECERATORY DIARRHEA

OSMOTIC DIARRHEA:

OSMOTIC DIARRHEA Stool output is proportional to the intake of the unabsorbable substrate and is usually not massive Diarrheal stools promptly regress with discontinuation of the offending nutrient, Stool ion gap is high, exceeding 100 mOsm /kg. Fecal osmolality in this circumstance is accounted for not only by the electrolytes but also by the unabsorbed nutrient(s) and their degradation products.

SECERATORY DIARRHEA:

SECERATORY DIARRHEA The epithelial cells’ ion transport processes are turned into a state of active secretion The most common cause of acute-onset secretory diarrhea is a bacterial infection of the gut. Features of secretory diarrhea include a high purg­ing rate, a lack of response to fasting, and a normal stool ion gap ( ie , 100 mOsm /kg or less), indicating that nutrient absorption is intact.

MECHANISM:

MECHANISM After colonization, enteric pathogens may adhere to or invade the epithelium; they may produce enterotoxins ( exotoxins that elicit secretion by increasing an intracellular second messenger) or cytotoxins . They may also trigger release of cytokines attracting inflammatory cells, which, in turn, contribute to the acti­vated secretion by inducing the release of agents such as prostaglandins or platelet-activating factor.

BACTERIAL DIARRHEA:

BACTERIAL DIARRHEA Campylobacter Salmonella Shigella Escherichia coli Cholera

Campylobacter:

Campylobacter Most common bacterial pathogen Incubation period 3 days(1-7 days) Transmitted through ingestion of contaminated food or by direct contact with fecal material,poultry , milk & tap water Symptoms include diarrhea (+/- blood), abdominal cramps (can be severe), malaise, fever Diagnosis by Stool culture

PowerPoint Presentation:

Usually self-limited and does not require antibiotics Azithromycin , 500 mg once a day for 3 days; Erythromycin, 500 mg four times a day for 3 days

SHIGELLA:

SHIGELLA Non-motile Does not ferment lactose Gas is not produced from glucose fermentation IMViC is -+-- Does not produce lysine decarboxylase H2S and urease negative

SPECIIES :

SPECIIES Sh. Dysenteriae . 10 – serotype(most serious) Sh. Flexenri . 6 – sero . Sh. Boydii . 15 - sero . Sh . sonnei . 1 - sero

PATHOGENESIIS:

PATHOGENESIIS Enteroinvasive – Colonic mucosa – Tissue damage –ulcers Exotoxin ( shiga toxin ) – sh. Dysenteriae – Enterotoxin (absorption) – Cytotoxin ( a – 5 b) – Neurotoxin (nerve damage)

PowerPoint Presentation:

B - subunit ----- glycolipids A – subunit----- 60s ribosomal Subunit. Inactivation inhibition Of protein synthesis . – cell death

Shigellosis:

62 Shigellosis within 2-3 days epithelial cell damage Gut lumen

SHIGELLOSIS:

SHIGELLOSIS • S. dysenteriae produces a neurotoxin called shiga toxin, which produces a severe syndrome • Shigellosis consists of a dysenteric syndrome – Bacillary dysentery – Invasive virulence mechanism • Incubation period of 7 h to 7 days – ~36 h in foodborne shigellosis • Low infective dose – 10-100 cells

CLINICAL FEATURES:

CLINICAL FEATURES Fever Bloody diarrhoea (red current jelly) Abdominal cramps Tenesmus Mucus , pus Convulsions Mild infection :watery stool Bacteremia - rare

COMPLICATIONS:

COMPLICATIONS Reiter,s syndrome Hemolytic – uremic syndrome Reactive arthritis Purulent keratoconjuncvitis Toxic megacolon Neurological manifestation like convulsions neuritis meningism & halluciations

DIAGNOSIS:

DIAGNOSIS 1 Culture Stool Rectal Swbs – Macconkey Agar Nlf – Dca ,, Xld – Selenite F Broth 2 Microscopy :: Leucocytes ,, Rbc 3 Biochemiical :: Tsi - No Gas,, H2s ,, Acid 4 Non Motile 5 Serology Test :: Slide agglutination test

TREATMENT:

TREATMENT Mild illness rehydratiion – SHORT ( 48 – 72 h) – Sh . sonnei Bacillary dysentery – Antimicrobial therapy 1. Ampcillin (plasmid resistance) 2. Cotrimoxazole (res..) 3. Ciprofloxacin 4. Azithromycin

Vibrio Cholera:

Vibrio Cholera Gram-negative Curved rod .5-.8 μ m width 1.4-2.6 μ m length Facultative anaerobe Single polar flagellum Chemoorganotroph Optimal growth 20-30 degrees

Pathogenesis of V. Cholera:

Pathogenesis of V. Cholera Cholera disease begins with ingestion of contaminated water or food. The bacteria that survive the acidic conditions of the stomach colonize in the small intestine. The cholera toxin (CT) is responsible for the severe diarrhea characteristic of the disease. Cholera Toxin CT is a proteinaceous enterotoxin secreted by V. Cholera

Cholera Toxin:

Cholera Toxin Structure Composed of a AB subunit. The B subunit forms a pentameric “doughnut” like structure that binds the CT to the receptor on the eukaryotic cells Pathway The A subunit contains the enzymatically active portion or the toxin Proteolytic cleavage of the A subunit results in A 1 and A 2 peptide units which remain linked by a disulfide bond Once the A subunit is internalized by the eukaryotic cell, the disulfide bond is reduced

Pathway continued:

Pathway continued The A 1 subunit contains a ADP-ribosyltransferase which covalently modifies the G protein, which regulates adenylate cyclase. Adenylate cyclase mediates the formation of cAMP The increase in cAMP levels bring about the secretion of chloride and bicarbonate from the mucosal cells into the intestinal lumen The change in ion concentrations leads to the secretion of large amounts of water into the lumen, known as diarrhea

Toxin Pathway Cartoon:

Toxin Pathway Cartoon

CLINICAL FEATURES:

CLINICAL FEATURES Incubation period 2-3 days Mild to severe disease is 1:1 with classical cholera and about 7:1 with EL tor vibrios Characteristic RICE WATER APPEARANCE of stools results from the presence of many flecks of mucus in clear fluid Pt complains of severe thirst Stool has faintly sweet or fishy odour

O/E:

O/E Patient has all signs of fluid loss( hypovoleamic shock) Kussmaul type of respiration if acidosis is not corrected Abdomen is nontender , scaphoid & bowel sounds diminished in frequency and intensity

CAUSE OF DEATH:

CAUSE OF DEATH Hypovoleamic shock Uncompensated Metabolic acidosis Renal failure due to ATN

DIAGNOSIS:

DIAGNOSIS By history Clinical examination Stool examination for rapidly motile vibrios by dark field illumination Isolation by cultre -A number of special media have been employed for the cultivation for cholera vibrios . These are

PowerPoint Presentation:

Holding or transport media Venkataraman-Ramakrishnan (VR) medium : This medium has 20g Sea Salt Powder and 5g Peptone dissolved in 1L of distilled water. Cary-Blair medium : This is the most widely-used carrying medium. This is a buffered solution of sodium chloride, sodium thioglycollate , disodium phosphate and calcium chloride at pH 8.4. Autoclaved sea water Enrichment media Alkaline peptone water at pH 8.6 Monsur's taurocholate tellurite peptone water at pH 9.2

PowerPoint Presentation:

Plating media Alkaline bile salt agar (BSA) : The colonies are very similar to those on nutrient agar . Monsur's gelatin Tauro cholate trypticase tellurite agar (GTTA) medium : Cholera vibrios produce small translucent colonies with a greyish black centre. TCBS medium : This the mostly widely used medium. This medium contains thiosulphate , citrate, bile salts and sucrose. Cholera vibrios produce flat 2–3 mm in diameter, yellow nucleated colonies.

MANAGEMENT:

MANAGEMENT ORS solution Up to 200ml/kg/day can be given on and avg In severe cases ORS is replaced by IV FLUIDS total fluid deficit is infused in 4 hrs and half of this in first hour. RL/Half NS fluids to be given Antibiotics

PowerPoint Presentation:

Treatment with a single dose of doxycycline , 300 mg or Treatment for 3 days with tetracycline, 500 mg 4 times daily or Single-dose treatment with fluoroquinolone .

VACCINES:

VACCINES An oral cholera vaccine is available, which gives immunity to 50-60% of those who take the vaccine, and this immunity lasts only a few months. Heat killed vaccine Used during epidemics

PREVENTION:

PREVENTION Safe drinking water and food “Boil it, cook it, peel it, or forget it. " Hand washing Proper sanitation

Pathogenesis:

Pathogenesis Infectious Dose: Shigella 10-100 organisms Campylobacter jejuni 10 (4) – 10 (6) organisms Salmonella 10 (5) – 10 (8) organisms Vibrio cholerae 10 (5) to 10 (8) organisms Enterotoxigenic E. coli 10 (8) organisms Yersinia enterocolitica 10(9) organisms EHEC (E. coli 0157: H7) 10-100 organisms

E COLI:

E COLI

PowerPoint Presentation:

1. At the species level, E. coli and Shigella are indistinguishable . Escherichia coli For practical reasons (primarily to avoid confusion), they are not placed in the same genus . There is a significant amount of overlap between diseases caused by the two organisms.

PowerPoint Presentation:

86 Enteropathogenic E. coli destruction of surface microvilli fever diarrhea vomiting nausea non-bloody stools Gut lumen

PowerPoint Presentation:

87 Enterotoxigenic E. coli Diarrhea Like Cholera Milder Travellers Diarrhea

Enterotoxigenic E. coli :

88 Enterotoxigenic E. coli Heat labile toxin like choleragen Adenyl cyclase activated cyclic AMP secretion water /ions Heat stable toxin Guanylate cyclase activated cyclic GMP uptake water /ions

PowerPoint Presentation:

89 Dysentery - resembles shigellosis Enteroinvasive E. coli (EIEC ) Gut lumen

PowerPoint Presentation:

90 Enterohemorrhagic E. coli Usually O157:H7 Transmission electron micrograph Flagella

Transmission – meat products or sewage-contaminated vegetables :

91 Transmission – meat products or sewage-contaminated vegetables Hemorrhagic bloody, copious diarrhea few leukocytes afebrile hemolytic-uremic syndrome hemolytic anemia thrombocytopenia (low platelets) kidney failure

Chronology of E. coli O157:H7 infections, an emerging type of foodborne illness. CDC :

Chronology of E. coli O157:H7 infections, an emerging type of foodborne illness. CDC 1982: First recognized as a pathoghen 1985: Associated with hemolytic uremic syndrome 1990: Outbreak from drinking water 1991: Outbreak from apple cider 1993: Multi-state outbread from fast food hamburgers 1995: Outbread from fresh produce 1996: Outbread in Japan Multi-state outbreak from unpasteurized apple juice

PowerPoint Presentation:

These organisms can produce a hemorrhagic colitis (characterized by bloody and copious diarrhea with few leukocytes in afebrile patients). However, they are taking increasing importance with the recognition of outbreaks caused by contaminated hamburger meat. The organisms can disseminate into the bloodstream producing systemic hemolytic-uremic syndrome (hemolytic anemia, thrombocytopenia and kidney failure).

PowerPoint Presentation:

Production of Vero toxin (biochemically similar to shiga toxin thus also known as "shiga-like") is highly associated with this group of organisms; encoded by a lysogenic phage. Hemolysins (plasmid encoded) are also important in pathogenesis.

PowerPoint Presentation:

95 Vero toxin “shiga-like” Hemolysins Enterohemorrhagic E. coli

Classification of Enteropathogenic E. coli:

Diarrhoea 2003, SGPGIMS, Lucknow Classification of Enteropathogenic E. coli Pathotype Clin Features Epidem. Features Virulence factors EPEC Watery diarr., vomiting Infants, Developing countries Bundle forming pilus, attaching-effacing EHEC Watery diarr., Hg. colitis Food & water borne Shiga toxins, attaching-effacing ETEC Watery diarr Childhood diarr., Traveler's diarr. Pili, ST & LT entero toxins EAEC Diarr with mucus Childhood diarr. Pili, cytotoxins EIEC Dysentery/ watery diarr Food borne Cellular invasion, intra cellular motility

E. coli:

E. coli Type Clinical Features Complications ETEC Watery diarrhea, travelers diarrhea rare EHEC Bloody diarrhea Hemolytic uremic syndrome, TTP (mostly 0157:H7) EIEC bloody diarrhea, dysentery rare EAEC Watery diarrhea or bloody diarrhea, mainly in children May be protracted

PowerPoint Presentation:

There are at least 4 etiologically distinct diseases caused by E. coli . The diagnostic laboratory generally does not differentiate the groups and treatment is based on symptomatology . Generally fluid replacement is the primary treatment. Antibiotics are generally not used except in severe disease or disease that has progressed to a systemic stage ( e.g.hemolytic -uremia syndrome).

PowerPoint Presentation:

Two major classes of pili are produced by E. coli ; mannose sensitive and mannose resistant pili . The former bind to mannose containing glyocoproteins and the latter to cerebrosides on the host epithelium allowing attachment. This aids in colonization by E. coli .

E. coli fimbriae:

100 E. coli fimbriae mannose Type 1 galactose glycolipids glycoproteins P

ANTIBIOTICS:

ANTIBIOTICS Fluroquinolones like ciprofloxcin,norfloxcin,levofloxcin Cotrimaxzole

Salmonella:

Salmonella

SALMONELLA:

103 SALMONELLA [417] Caption: Salmonella typhi - Gram-negative, enteric, rod prokaryote (dividing); causes typhoid fever. Magnification*: x5,530 Type: SEM Keywords: 96430B.TIF bacilli bacillus bacteria bacterial pathogen bacterium division Gram-negative human disease infection prokaryote rod Salmonella typhi typhoid fever enteric bacterial pathogen intestinal tract infection SEM |

Salmonella :

Salmonella Salmonella typhimurium - rod prokaryote (dividing); note the flagella. Causes salmonellosis (food poisoning). (x 20,800) © Dr Dennis Kunkel, University of Hawaii. Used with permission

Salmonella:

105 Salmonella 2000 antigenic "types” genetically single species S. enterica disease category S. enteritidis many serotypes S. cholerae-suis S. typhi

Salmonellosis:

106 Salmonellosis S. enteritidis the common salmonella infection poultry, eggs no human reservoir Gastroenteritis nausea vomiting non-bloody stool self-limiting (2 - 5 days)

Salmonellosis:

107 Salmonellosis uncomplicated cases (the vast majority) antibiotic therapy not useful Gut lumen

PowerPoint Presentation:

Like Shigella , salmonella invade the epithelium and do not produce systemic infection. In uncomplicated cases of salmonellosis , which are the vast majority, antibiotic therapy is not useful. S. cholerae-suis (seen much less commonly) causes septicemia after invasion. In this case, antibiotic therapy is required.

PowerPoint Presentation:

The severest form of salmonella infections is called "typhoid" or enteric fever. Typhoid is caused by Salmonella typhi . Typhoid is one of the historical causes of widespread epidemics and still causes epidemics in the third world.

Salmonella typhi:

Salmonella typhi The organism is transmitted from: 1. a human reservoir 2. in the water supply (if sanitary conditions are poor) 3 . in contaminated food It initially invades the intestinal epithelium and during this acute phase, gastrointestinal symptoms are noted.

PowerPoint Presentation:

The organisms penetrates (usually within the first week) and passes into the bloodstream where it is disseminated in macrophages. Typical features of a systemic bacterial infection are noted. The septicemia usually is temporary with the organism finally lodging in the gall bladder. Organisms are shed into the intestine for some weeks.

PowerPoint Presentation:

At this time the gastroenteritis (including diarrhea) is noted again. A carrier state is common; thus one person e.g. a food handler can cause a lot of spread. Antibiotic therapy is essential. Vaccines are not widely effective and not generally used. The Vi (capsular) antigen plays a role in the pathogenesis of typhoid.

PowerPoint Presentation:

Isolation Rate for Salmonella enteritidis by Region, United States, 1974-1994 CDC

Classic Syndromes: Travelers Diarrhea:

Classic Syndromes: Travelers Diarrhea Attack rates of as high as 25% 90% brief and self-limited Persistent diarrhea in 1-2% Depends on destination, eating habits, length of stay Pathogen % ETEC 40 EAEC 15 C. jejuni 10 Shigella 10 EHEC or EIEC <5 Salmonella < 5 Vibrio < 5

Food-borne illness:

Food-borne illness Agent % Norwalk 45 C. perfringens 12 Salmonella 11 S. aureus 4 EHEC (0157) 4 C. jejuni 4 B. cereus 2 Shellfish-borne % Norwalk 52 Vibrio 37 Salmonella <1 Other 10

Nosocomial diarrhea:

Nosocomial diarrhea Clostridium difficle Increasing worldwide due to hypervirulent strain (North American Pulsefield type 1) High fluoroquinolone resistance Less responsive to usual therapy (metronidazole) Higher complication rate

PowerPoint Presentation:

Pathobiology /Agents Incubation Period Vomiting Abdominal Pain Fever Diarrhea Toxin producers Bacillus cereus , Staphylococcus aureus , 1–8 h 3–4+ 1–2+ 0–1+ 3–4+, watery Clostridium perfringens 8–24 h Enterotoxin Vibrio cholerae , enterotoxigenic Escherichia coli , Klebsiella pneumoniae , Aeromonas species 8–72 h 2–4+ 1–2+ 0–1+ 3–4+, watery Enteroadherent Enteropathogenic and enteroadherent E. coli , Giardia organisms, cryptosporidiosis, helminths 1–8 d 0–1+ 1–3+ 0–2+ 1–2+, watery, mushy Cytotoxin-producers Clostridium difficile 1–3 d 0–1+ 3–4+ 1–2+ 1–3+, usually watery, occasionally bloody Hemorrhagic E. coli 12–72 h 0–1+ 3–4+ 1–2+ 1–3+, initially watery, quickly bloody Variable inflammation Salmonella , Campylobacter , and Aeromonas species, Vibrio parahaemolyticus , Yersinia 12 h–11 d 0–3+ 2–4+ 3–4+ 1–4+, watery or bloody Severe inflammation Shigella species, enteroinvasive E. coli , Entamoeba histolytica 12 h–8 d 0–1+ 3–4+ 3–4+ 1–2+, bloody

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